普罗布考对糖尿病兔心房重构及心房颤动发生的影响
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摘要
背景：糖尿病是心房颤动(房颤)发生的独立危险因素之一,糖尿病引起房颤发生的机制尚不明确。研究表明,炎症和氧化应激在糖尿病及房颤的发生发展过程中都发挥了重要作用。由此推测,炎症和氧化应激可能是糖尿病引起房颤的作用通路。
目的：为了探讨糖尿病房颤发生的机制,以及抗炎抗氧化药物普罗布考对糖尿病房颤发生的作用,本研究从整体水平、细胞离子通道水平及分子生物学水平探讨糖尿病引起的心房结构性重构和电重构,评价普罗布考的干预作用及其可能机制。
方法：共三部分实验,每部分应用健康成年日本大耳白兔40只,随机分为四组：对照组(Control, C组),糖尿病组(Diabetes mellitus, DM组),普罗布考组(Control+probucol, CPR组)和糖尿病普罗布考组(DM+probucol, DPR),每组10只。四氧嘧啶兔耳缘静脉以120mg/kg注射建立糖尿病模型,DPR及CPR组予普罗布考(1000mg/d),饲养8周。8周后完成以下三部分实验：1.建立Langendorff灌流的离体兔心脏模型,测量心房间传导时间(IACT)、心房各点有效不应期(AERP)、AERP的离散度(AERPD)、应用Burst刺激观察房颤诱发情况,应用天狼猩红染色评价左房纤维化情况,检测血清中过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子-a(TNF-α)和髓过氧化物酶(MPO)水平。2.采用酶解的方法分离单个心房肌细胞,采用全细胞膜片钳技术记录L型钙电流(ICa,L),钠电流(INa)及动作电位。3.左心房肌组织行RT-PCR及Western Blotting研究,比较四组TNF-α和TLR4的基因表达以及Cav1.2、NF-κB、ERK、P-ERK,TGF-β和HSP70的蛋白表达的不同。
结果：与C组相比,DM组IACT延长(36.55±6.4ms vs25.75±2.7ms,P<0.05),AERPD增大(28.37±7.52ms vs11.62±5.60ms,P<0.05)房颤诱发率升高(8/10vs1/10,P<0.05)；病理检查提示DM组心房肌细胞横截而积增大(131.51±14.69μm2vs105.90±15.67μm2,P<0.05),左房心肌间质明显纤维化(6.86±1.71%vs2.13±0.75%,P<0.05),MDA(22.17±4.15nmo1/ml vs17.69±3.59nmol/ml,P<0.05),TNF-α水平增高(334.15±84.94pg/ml vs226.48±46.01pg/ml,P<0.05)；DM组ICa,L最大电流密度增大(8.94±3.81pA/pF vs5.16±1.10pA/pF,P<0.05),INa最大电流密度减小(86.75±17.55pA/pF vs120.00±13.11pA/p F,P<0.05),动作电位时程(APD)90及APD50延长。糖尿病组Cav1.2,TNF-α,TLR4基因表达增多,NF-κB,ERK, P-ERK,TGF-β,HSP70蛋白表达增加。与DM组相比,DPR组IACT缩短(23.87±1.64ms vs36.55±6.4ms,P<0.05),AERPD减小(?)(15.62±7.65vs28.37±7.52,P<0.05),房颤诱发率明显减低(3/10vs8/10,P<0.05),心肌细胞横截面积减小(120.85±8.27μm2vs131.51±14.69μm2,P<0.05),心肌纤维化减轻,胶原容积分数减小(?)(3.41±1.27%vs6.86±1.71％,P<0.05),MDA,TNF-α水平减低,ICa,L最大电流密度减小(6.51±1.25pA/pF vs8.94±3.81pA/pF,P<0.05),INa最大电流密度增大(137.0±28.59pA/pF vs86.75±17.55pA/pF,P<0.01),APD90及APD50缩短。TNF-α,TLR4的基因表达及NF-κB,TGF-p,HSP70的蛋白表达下调。而CPR与C组比较组未发现离子通道特性和蛋白表达的明显改变。
结论：糖尿病引起心房重构机制为NF-κB活化,NF-κB活化过程的介质和产物(如TGF-β,TLR4等)是引起糖尿病炎症、心肌细胞肥大以及心房纤维化的原因,构成房颤发生的基质。糖尿病引起的氧化应激可能是心肌细胞离子通道电流改变ICa,L电流密度增大,INa电流密度减小的主要原因。离子通道改变,导致电活动的不稳定,房颤诱发率增高。普罗布考通过抗炎抗氧化作用减轻糖尿病引起的电重构和结构重构,减少房颤发生。
Objective Diabetes mellitus (DM) is an independent risk factor for atrial fibrillation (AF) and has been recognized as a low-grade inflammation disease. Inflammation has also been shown to have a direct role in the initiation, maintenance, and recurrence of AF. On the other hand, oxidative stress play critical role in the pathophysiology of DM and the development of vascular complications, which may also relate to the development of AF. So we hypotheses that inflammation and oxidative stress may be important mechanisms for the increased propensity for AF in DM. The purpose of this study was to elucidate the underlying mechanisms of AF and to evaluate the effects of probucol on atrial electrophysiological changes and AF promotion in alloxan-induced diabetic rabbits.
Methods The experiment was divided into three parts. In each part,40Japanese rabbits were randomly assigned to a normal control group (C, n=10), a alloxan-induced diabetic group (DM, n=10), probucol-treated group (CPR, n=10) and probucol-treated diabetic group (DPR, n=10). In the DM and DPR group, alloxan monohydrate was immediately administered intravenously via the marginal ear vein. Rabbits in the DPR and CPR groups were orally administered Probucol (1000mg/day) for8weeks. The animals in four groups were housed in cages and a standard laboratory pellet diet for8weeks. In part one, isolated Langendorff perfused rabbit hearts were prepared to evaluate atrial refractory effective period (AERP) and its dispersion (AERPD), interatrial conduction time (IACT) and vulnerability to AF. Plasma malonaldehyde (MDA), superoxide dismutase (SOD), TNF-a, myeloperoxidase(MPO) and catalase (CAT) levels were measured by chemical colourimetric methods. Sirius-Red staining was used to evaluate atrial fibrosis. In part two, using whole-cell voltage-clamp techniques,Ica,L,INa and action potential(AP) were measured in left atrial myocytes isolated from the rabbits of four groups. In part three, the expression levels of Cavl.2, NF-κB, ERK, P-ERK, TGF-β and HSP70in left atrial tissue were analysed by western blot, the expression levels of TNF-a and TLR4were analysed by RT-PCR methods.
Results IACT and AERPD were prolonged in diabetic rabbits compared with controls. Inducibility of AF in diabetic group was significant higher than controls (8/10vs1/10, P<0.05). Extensive interstitial fibrosis was observed in the DM group (P<0.05). Plasma MDA and TNF-a were increased significantly in the DM group (P<0.05). The density of Ica,L current in diabetic myocytes was significantly higher than that in the control, the density of INA current was significantly decreased in diabetic myocytes. APD90and APD50were also prolonged in diabetic myocytes. NF-κB, ERK, P-ERK, TGF-β and HSP70protein and the levels of Cavl.2, TNF-a mRNA and TLR4mRNA expression were significantly upregulated in DM group. The DPR rabbits exhibited significant alleviation of oxidative stress displayed as decreased plasma MDA and TNF-a compared with diabetic rabbits (P<0.05), probucol administration increases stability of vulnerable atrial fibrillation in diabetic rabbits (P<0.05). Histological analysis revealed suppression of DM-related histological changes (interstitial fibrosis) by probucol. The density of iCa,L current was significantly decreased and the density of INa current was significantly increased in DPR myocytes. Probucol significantly downregulated atrial NF-κB, TGF-β and HSP70protein expression and TNF-a mRNA and TLR4mRNA expression in DPR left atrial tissue.
Conclusion There is an increased NF-κB activity in diabetes mellitus. Some of target cytokines NF-κB controls and stimulus of NF-κB like TGF-β, TLR4are responsible for inflammation, atrial fibrosis and hypertrophy of atrial tissue, which may serve as an important substrate for the development of AF. Alterations of atrial Ica,L and INa were due to the increased oxidative stress, which lead to the unstablity of electrical activity and subsequent occurrence of AF. Probucol through its powerful anti-inflammatory and antioxidant activity preserves the structural integrity of atrial tissues and increases stability of vulnerable atrial fibrillation in alloxan-induced diabetic rabbits.
目的：为了探讨糖尿病房颤发生的机制,以及抗炎抗氧化药物普罗布考对糖尿病房颤发生的作用,本研究从整体水平、细胞离子通道水平及分子生物学水平探讨糖尿病引起的心房结构性重构和电重构,评价普罗布考的干预作用及其可能机制。
方法：共三部分实验,每部分应用健康成年日本大耳白兔40只,随机分为四组：对照组(Control, C组),糖尿病组(Diabetes mellitus, DM组),普罗布考组(Control+probucol, CPR组)和糖尿病普罗布考组(DM+probucol, DPR),每组10只。四氧嘧啶兔耳缘静脉以120mg/kg注射建立糖尿病模型,DPR及CPR组予普罗布考(1000mg/d),饲养8周。8周后完成以下三部分实验：1.建立Langendorff灌流的离体兔心脏模型,测量心房间传导时间(IACT)、心房各点有效不应期(AERP)、AERP的离散度(AERPD)、应用Burst刺激观察房颤诱发情况,应用天狼猩红染色评价左房纤维化情况,检测血清中过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子-a(TNF-α)和髓过氧化物酶(MPO)水平。2.采用酶解的方法分离单个心房肌细胞,采用全细胞膜片钳技术记录L型钙电流(ICa,L),钠电流(INa)及动作电位。3.左心房肌组织行RT-PCR及Western Blotting研究,比较四组TNF-α和TLR4的基因表达以及Cav1.2、NF-κB、ERK、P-ERK,TGF-β和HSP70的蛋白表达的不同。
结果：与C组相比,DM组IACT延长(36.55±6.4ms vs25.75±2.7ms,P<0.05),AERPD增大(28.37±7.52ms vs11.62±5.60ms,P<0.05)房颤诱发率升高(8/10vs1/10,P<0.05)；病理检查提示DM组心房肌细胞横截而积增大(131.51±14.69μm2vs105.90±15.67μm2,P<0.05),左房心肌间质明显纤维化(6.86±1.71%vs2.13±0.75%,P<0.05),MDA(22.17±4.15nmo1/ml vs17.69±3.59nmol/ml,P<0.05),TNF-α水平增高(334.15±84.94pg/ml vs226.48±46.01pg/ml,P<0.05)；DM组ICa,L最大电流密度增大(8.94±3.81pA/pF vs5.16±1.10pA/pF,P<0.05),INa最大电流密度减小(86.75±17.55pA/pF vs120.00±13.11pA/p F,P<0.05),动作电位时程(APD)90及APD50延长。糖尿病组Cav1.2,TNF-α,TLR4基因表达增多,NF-κB,ERK, P-ERK,TGF-β,HSP70蛋白表达增加。与DM组相比,DPR组IACT缩短(23.87±1.64ms vs36.55±6.4ms,P<0.05),AERPD减小(?)(15.62±7.65vs28.37±7.52,P<0.05),房颤诱发率明显减低(3/10vs8/10,P<0.05),心肌细胞横截面积减小(120.85±8.27μm2vs131.51±14.69μm2,P<0.05),心肌纤维化减轻,胶原容积分数减小(?)(3.41±1.27%vs6.86±1.71％,P<0.05),MDA,TNF-α水平减低,ICa,L最大电流密度减小(6.51±1.25pA/pF vs8.94±3.81pA/pF,P<0.05),INa最大电流密度增大(137.0±28.59pA/pF vs86.75±17.55pA/pF,P<0.01),APD90及APD50缩短。TNF-α,TLR4的基因表达及NF-κB,TGF-p,HSP70的蛋白表达下调。而CPR与C组比较组未发现离子通道特性和蛋白表达的明显改变。
结论：糖尿病引起心房重构机制为NF-κB活化,NF-κB活化过程的介质和产物(如TGF-β,TLR4等)是引起糖尿病炎症、心肌细胞肥大以及心房纤维化的原因,构成房颤发生的基质。糖尿病引起的氧化应激可能是心肌细胞离子通道电流改变ICa,L电流密度增大,INa电流密度减小的主要原因。离子通道改变,导致电活动的不稳定,房颤诱发率增高。普罗布考通过抗炎抗氧化作用减轻糖尿病引起的电重构和结构重构,减少房颤发生。
Objective Diabetes mellitus (DM) is an independent risk factor for atrial fibrillation (AF) and has been recognized as a low-grade inflammation disease. Inflammation has also been shown to have a direct role in the initiation, maintenance, and recurrence of AF. On the other hand, oxidative stress play critical role in the pathophysiology of DM and the development of vascular complications, which may also relate to the development of AF. So we hypotheses that inflammation and oxidative stress may be important mechanisms for the increased propensity for AF in DM. The purpose of this study was to elucidate the underlying mechanisms of AF and to evaluate the effects of probucol on atrial electrophysiological changes and AF promotion in alloxan-induced diabetic rabbits.
Methods The experiment was divided into three parts. In each part,40Japanese rabbits were randomly assigned to a normal control group (C, n=10), a alloxan-induced diabetic group (DM, n=10), probucol-treated group (CPR, n=10) and probucol-treated diabetic group (DPR, n=10). In the DM and DPR group, alloxan monohydrate was immediately administered intravenously via the marginal ear vein. Rabbits in the DPR and CPR groups were orally administered Probucol (1000mg/day) for8weeks. The animals in four groups were housed in cages and a standard laboratory pellet diet for8weeks. In part one, isolated Langendorff perfused rabbit hearts were prepared to evaluate atrial refractory effective period (AERP) and its dispersion (AERPD), interatrial conduction time (IACT) and vulnerability to AF. Plasma malonaldehyde (MDA), superoxide dismutase (SOD), TNF-a, myeloperoxidase(MPO) and catalase (CAT) levels were measured by chemical colourimetric methods. Sirius-Red staining was used to evaluate atrial fibrosis. In part two, using whole-cell voltage-clamp techniques,Ica,L,INa and action potential(AP) were measured in left atrial myocytes isolated from the rabbits of four groups. In part three, the expression levels of Cavl.2, NF-κB, ERK, P-ERK, TGF-β and HSP70in left atrial tissue were analysed by western blot, the expression levels of TNF-a and TLR4were analysed by RT-PCR methods.
Results IACT and AERPD were prolonged in diabetic rabbits compared with controls. Inducibility of AF in diabetic group was significant higher than controls (8/10vs1/10, P<0.05). Extensive interstitial fibrosis was observed in the DM group (P<0.05). Plasma MDA and TNF-a were increased significantly in the DM group (P<0.05). The density of Ica,L current in diabetic myocytes was significantly higher than that in the control, the density of INA current was significantly decreased in diabetic myocytes. APD90and APD50were also prolonged in diabetic myocytes. NF-κB, ERK, P-ERK, TGF-β and HSP70protein and the levels of Cavl.2, TNF-a mRNA and TLR4mRNA expression were significantly upregulated in DM group. The DPR rabbits exhibited significant alleviation of oxidative stress displayed as decreased plasma MDA and TNF-a compared with diabetic rabbits (P<0.05), probucol administration increases stability of vulnerable atrial fibrillation in diabetic rabbits (P<0.05). Histological analysis revealed suppression of DM-related histological changes (interstitial fibrosis) by probucol. The density of iCa,L current was significantly decreased and the density of INa current was significantly increased in DPR myocytes. Probucol significantly downregulated atrial NF-κB, TGF-β and HSP70protein expression and TNF-a mRNA and TLR4mRNA expression in DPR left atrial tissue.
Conclusion There is an increased NF-κB activity in diabetes mellitus. Some of target cytokines NF-κB controls and stimulus of NF-κB like TGF-β, TLR4are responsible for inflammation, atrial fibrosis and hypertrophy of atrial tissue, which may serve as an important substrate for the development of AF. Alterations of atrial Ica,L and INa were due to the increased oxidative stress, which lead to the unstablity of electrical activity and subsequent occurrence of AF. Probucol through its powerful anti-inflammatory and antioxidant activity preserves the structural integrity of atrial tissues and increases stability of vulnerable atrial fibrillation in alloxan-induced diabetic rabbits.
引文
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